ARRHYTHMIA

 Any changes from normal sequence of electrical impulses – too fast, too slow or
erratically which can lead to improper contraction of the heart.

NORMAL ELECTRICAL CONDUCTANCE OF THE HEART

 PR interval: electrical signal reach AV node

 Q wave: electrical signal passed Bundle of His -> left and right bundle branches.
 Q-R: contraction of left ventricle
 R-S: contraction of right ventricle

U wave: if too prominent; suspect hypokalemia, hypercalcemia and hyperthyroidism.

TYPE
 Atrial fibrillation
 Most common, very fast and irregular contraction of the atria.
 Signal not begin in SA node but start at another part in the atria/nearby
pulmonary vein -> electrical signal not travel normally-> atrial fibrillate->
not able to pump blood into ventricular ->create pool of blood->thrombus->
stroke.
 ECG
 P wave absence
 P-R interval irregular
 QRS complex narrow.

 Complication
 Stroke
 Heart failure
 Treatment
 Prevent stroke
 Restored heart rhythm/ rate

 Ventricular fibrillation
 Lower chamber quiver and the heart cannot pump any blood -> cardiac
arrest -> medical emergency.
 Disorganized electrical signal make ventricle quiver instead of pump
normally -> give electrical shock (defibrillation)
  Sign

 Loss of responsiveness
 Abnormal breathing
 Cardiac arrest
 ECG
 Rate : rapid and disorganized to count
 No discernible organized waves at all
 Torsade de Pointes (twisting of the point)
 unique pattern of V-fib
 rapid, polymorphic ventricular tachycardia with a
characteristic twist of the QRS complex around isoelectrical
baseline

 Bradycardia
 < 60 b/m
 Due to
 Heart Attack
 Disturb the electrical activity
 Imbalance of potassium in blood
 Medication
 Symptom
 Fatigue
 Dizziness
 Lightheadedness
 Fainting
 Cardiac arrest
  Complication
 Heart
 Syncope
 Angina pectoris
 Increase BP (reflex)
 ECG
 Rate : <60 bpm
 Rhythm : regular

 Tachycardia
 Fast heart rate that starts in the ventricle
 Electrical signal in the ventricle fire abnormally ->interfere with electrical
signal coming from SA node ->increase heart beat -> not allow filling time
-> decrease cardiac output.
 ECG
 3 or more beats of ventricular origin - > 100 bpm
 Rhythm: regular
 P wave not seen
 QRS complex widen.

 Conductance disorder
 Bundle branch block
 Right BBB
- Transmission of the electrical impulse is delayed or not
conducted along the right bundle branch.
- The right ventricle depolarizes by means of cell-to-cell
conduction that spreads from the interventricular septum and
left ventricle to the right ventricle.
 Left BBB
- Transmission of the cardiac electrical impulse is delayed or
fails to be conducted along the rapidly conducting fibers of
the main left bundle branch or in both left anterior and
posterior fascicles.
- the left ventricle slowly depolarizes by means of cell-to-cell
conduction that spreads from the right ventricle to the left
ventricle
 Heart block
 First degree heart block
 Electrical impulse moves through the AV node more slowly
than normal.
 ECG – PR interval longer than 2 second
 Second degree heart block
 some electrical signal from atria don’t reach the ventricle->
‘dropped beat’
 P wave is blocked from initiating a QRS complex
 Type I
- Increase delay in each cycle before the omission.
- Progressive prolongation of the PR interval then
followed by blocked P wave (dropped QRS)
 Type II
- an unexpected nonconducted atrial impulse
-  the PR and R-R intervals between conducted beats
are constant

 Third degree heart block

 Heart electrical impulse does not pass from the heart’s upper
to lower chamber at all -> secondary pacemaker cell -> take
over-> heart contract at slower rate.
 ECG
- P wave present but no relation whatsoever with QRS
complex
- PR interval are irregularly irregular
- QRS complex widen
 - Complete absent of conduction between atria and
ventricular.

 Long QT syndrome
 Delay repolarization of the heart following a heartbeat -> increase
risk of Torsade de Pointes.
 Abnormal repolarizations cause differences in the refractory period
of the myocytes.
 Due to re-opening of L-type Ca2+ channel during platue phase of
the cardiac action potential -> increase Ca2+ filling of the
sarcoplasmic reticulum -> spontaneous release during
repolarization ->net depolarization current.

 Premature contraction
 Premature atrial contractions (PAC) and Premature ventricular
contractions (PVC)
 Most common
 Fluttering in the chest / skipped beat
 Not required treatment
 Due to stress, caffeine, nicotine and exercise.

 Other rhythm disorder

 Adam stokes disease
 Temporary condition that leads to fainting/syncope
 Caused by slow-firing SA node ->bradycardia
 Atrial flutter
 Travel fast and regular rhythm ; > 100bpm
 Due to reentrant rhythm (Left/right) -> premature electrical impulse
arising in the atria -> different in refractory period of atrial tissue.
 ECG
- Saw-tooth appearance (P wave)
- R-R interval normal
- QRS normal

 Sick sinus syndrome

 Sick sinus syndrome is a collection of heart rhythm disorders that

include:
- Sinus bradycardia -- slow heart rates from the natural
pacemaker of the heart
- Tachycardias -- fast heart rates
- Bradycardia-tachycardia -- alternating slow and fast heart
rhythms
 Sinus arrhythmia
 As the anxious state of the slowing down of the heart while
breathing out or during expiration and increasing of the heart beat
while inhaling or during inspiration.
 Affects the vagus nerve which is responsible for activating the
nervous system-triggered parasympathetic input which regulates
the heart beat. In simple words, the vagus nerve is left unstimulated
resulting in the wrong signals to the heart and the subsequent
decline in pitch of the heart rate.

 Wolff-Parkinson-White syndrome
 Preexcitation of the ventricle of the heart -> Bundle of Kent ->
create an electrical circuit that bypass the AV node ->
tachyarrhythmia.
 Classic ECG findings that are associated with WPW syndrome
include the following:
- Presence of a short PR interval (< 120 ms)
- A wide QRS complex longer than 120 ms with a slurred
onset of the QRS waveform producing a delta wave in the
early part of QRS
- Secondary ST-T wave changes
CAUSES
 Natural pacemaker develop an abnormal rate of rhythm
 Normal conductance pathway are interrupted
 Another part of the heart takes over as pacemaker
 Smoking, alcohol, certain drugs ( indirect)
 Increase BP, stress, heart attack
ARRHYTHMIA MATTER
 Cardiac arrest
 Scarring from a prior heart attack
 Cardiomyopathy
 Heart medication- proarrhytmia effect (change in K and Mg)
 Electrical abnormal
 Blood vassel abnormal

 Stroke
 Artial fibrillation

RISK FACTORS
 Heart attack
 Heart failure (cardiomyopathy)
 Leaking/narrowing of heart valves
 Congenital heart defect
 Increase BP
 Infection
 Diabetes
 Over/ underproduction of thyroid hormone

SIGN AND SYMPTOM

 Palpitation
 Slow/fast heart beat
 Irregular heart beat
 Paused between heart beat
 Anxiety
 Weakness, dizziness and lightheadedness
 Fainting
 Sweating
 SOB and chest pain
DIAGNOSIS
 Family history and physical examination
 ECG
 Holter and event monitor
 Coronary angiograpy
 Blood test (K+ and thyroid hormone)
 Chest X-ray
 Echocardiography
 Stress test

TREATMENT
 Medication
 Anti-arrhythemia
 Beta-blocker (metaprolol, atenolol)
 Ca2+ channel blocker (verapamil,diltiazem)

 Restore normal heart beat

 Amiodarone
 Sotalol
 dronedarone
 Anti-coagulant
 Aspirin

 Medical procedure
 Pacemaker
 Defibrillation/cardioversion
 Implantable cardioverter defibrillation (ICD)
 Catheter ablation

 Surgery
 Repair heart valve
 Maze surgery
 Coronary artery bypass grafting